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. 2024 Jun 18;13:62. doi: 10.1186/s40164-024-00527-1

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© The Author(s) 2024

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 4 — The pro-inflammatory and anti-inflammatory effects of IL-6 in the liver pathological process. The overexpression of IL-6 induced by liver injury presents a double-edged sword effect on the hepatic pathological process. Its pro-inflammatory effect promotes liver steatosis, fibrosis, endothelial cells (ECs) proliferation, and HCC development. On the other side, liver injury or chronic hepatitis are promoted in IL-6 or STAT3 knockout mice, suggesting the anti-inflammatory effect of IL-6. Moreover, IL-6 secreted by liver stroma cells can induce the differentiation of recruited monocytes towards tissue-resident Kupffer cells, but away from SAMs, so as to limit hepatic inflammation